The notion that the lumen of the ATP synthase membrane rotor is the long-sought megachannel that triggers the onset of the mitochondrial permeability transition is found to be inconsistent with its actual structural and functional properties.
Loss of the F-ATP synthase c-subunit inhibits a pathological mitochondrial permeability transition pore that is coupled to a maladaptive mitochondrial unfolded protein response while also extending lifespan.
Correlative microscopy and electron cryo-tomography on apoptotic HeLa cells reveal remodeling of outer and inner mitochondrial membranes, Bax cluster ultrastructure and ATP synthase reorganization in ruptured mitochondria.
TORC2-Ypk1 signaling upregulates flux through the sphingolipid pathway not only by increasing the supply of long-chain base precursors, but also by increasing their use in synthesizing complex sphingolipids.
Changes in pathways of lipid oxidation, glycolysis, and mitochondrial oxidative phosphorylation are common strategies to cope with high-altitude hypoxia, but some changes require longer evolutionary time to arise.
A novel dimethylsulfoniopropionate lyase was identified, which catalyzes dimethyl sulfide releasing by a new mechanism and is found in several bacterial lineages, revealing its important roles in global sulfur cycling.
Mitochondrial electron transport chain dysfunction triggers the integrated stress response due to an asparagine deficiency downstream of impaired NADH oxidation in proliferating myoblasts, but not in differentiated myotubes.